TREATMENT OF ATHLETES

Treating participants in athletics requires the coordination of coaches, trainers, administrators and physician. Often in cases of proneness to injury, a cause can be found and correction may be obtained by further training or withdrawal of the athlete from the team.Certain types of injury should be always kept in mind in the examination of athletes, particularly football players. Ligamentous tears, myositis ossificans, navicular fracture and brain injury are injuries that may not be precisely diagnosed at the initial examination.     

FRACTURES AND DISLOCATIONS OF THE CARPUS

Although one-eighth to one-tenth of all fractures of the wrist are carpal fractures, they may be overlooked, unless attention is directed particularly to them in diagnostic examination. Symptoms may be slight or lacking, but diagnosis is important because such injuries may give rise to pain or disability later. There are certain guides and procedures in physical and roentgenographic examination which make diagnosis easier and more certain. Treatment depends upon the nature of the lesion. It must be based on all the knowledge obtainable by examination, mental review of the anatomy and pathologic changes, inquiry into the cause of injury, and the interpretation of roentgenologic findings.     

Biomechanical assessment of the effects of significant hamstring injury: an isokinetic study

Soccer players may develop recurrent hamstring injuries. This may be due to inadequate rehabilitation or to recurrent injury. In addition, following injury, the hamstring muscular complex may be permanently damaged, resulting in decreased strength, and increased likelihood of recurrent injury. Fourteen professional soccer players were assessed by clinical examination and by isokinetic testing with a Cybex II machine. Seven had suffered moderate or major hamstring injuries in the past year. There were seven controls. None of the hamstring group were currently suffering from an acute hamstring injury. The results of the two groups were compared. There were no differences in the mean results. This pilot study suggests that no permanent functional damage occurs to the muscular complex after moderate or major hamstring injuries after correct treatment. However, further research is required to confirm this.     

Liver inflammation and cytokine production, but not acute phase protein synthesis, accompany the adult liver progenitor (oval) cell response to chronic liver injury

Oval cells are facultative liver progenitor cells, which are invoked during chronic liver injury in order to replenish damaged hepatocytes and bile duct cells. Previous studies have observed inflammation and cytokine production in the liver during chronic injury. Further, it has been proposed that inflammatory growth factors may mediate the proliferation of oval cells during disease progression. We have undertaken a detailed examination of inflammation and cytokine production during a time course of liver injury and repair, invoked by feeding mice a choline-deficient, ethionine-supplemented (CDE) diet. We show that immediately following initial liver injury, B220-expressing leucocytes transiently infiltrate the liver. This inflammatory response occurred immediately before oval cell numbers began to expand in the liver, suggesting that the two events may be linked. Two waves of liver cytokine production were observed during the CDE time course. The first occurred shortly following commencement of the diet, suggesting that it may represent a hepatic acute phase response. However, examination of acute phase marker expression in CDE-fed mice did not support this hypothesis. The second wave of cytokine expression correlated with the expansion of oval cell numbers in the liver, suggesting that these factors may mediate oval cell proliferation. No inflammatory signalling was detected following withdrawal of the injury stimulus. In summary, our results document a close correlation between inflammation, cytokine production and the expansion of oval cells in the liver during experimental chronic injury.     

INITIAL CARE OF ACUTE BACK INJURIES

The mechanism of injury to the back should be obtained with the utmost accuracy and set down in the history as a separate paragraph under that heading. This is usually best obtained by questioning and requestioning the patient during the course of the examination. A history of any previous back affections should also be obtained at the first visit.The detailed examination of the back is not complete without a general physical examination.X-ray studies should be done immediately in all cases in which the injury has been caused by direct violence or forceful indirect violence (as in “jackknife” injury).Terms such as “disc disease,” “ruptured intervertebral disc” and various others that convey a similar meaning should not be used as the initial diagnosis and should be withheld until such a diagnosis is definitely established.The plan of treatment may include a period in hospital or of rest at home, or it may be carried out with the patient ambulatory. Corsets and braces should be prescribed only when they are to serve a definite function and the same can be said of physiotherapy.     

The Management of Abdominal Injuries in the Presence of Head Injury

When head and blunt abdominal injuries are combined, the head injury is often afforded too much attention and the abdominal injury too little, especially when the patient is unconscious. If mismanaged, the abdominal injury is often the more serious threat to life. Except for extradural hemorrhage, neurosurgical intervention, when indicated, can be delayed until the patient has been thoroughly evaluated for the presence of extra cranial injuries with higher therapeutic priority.Abdominal examination of the unconscious or uncooperative patient is difficult. Tenderness as a sign of abdominal injury cannot be elicited. Abdominal rigidity (in the absence of rigid extremities), a silent abdomen, shock, and extreme restlessness may indicate intra-abdominal changes. Abdominal paracentesis is a valuable diagnostic aid, and the finding of blood, bile-stained fluid, intestinal contents or air is an indication for immediate laparotomy. Once all injuries are known, priorities for treatment can be assigned. Often head and abdominal injuries can be treated concomitantly.     

Adult peripheral nerve disorders: nerve entrapment, repair, transfer, and brachial plexus disorders

LEARNING OBJECTIVES: After reading this article, the participant should be able to: 1. Describe the pathophysiologic bases for nerve injury and how they apply to patient evaluation and management. 2. Recognize the wide variety of injury patterns and associated patient complaints and physical findings associated with peripheral nerve pathology. 3. Evaluate and recommend further tests to aid in defining the diagnosis. 4. Specify treatment options and potential risks and benefits. SUMMARY: Peripheral nerve disorders comprise a gamut of problems, ranging from entrapment neuropathy to direct open traumatic injury and closed brachial plexus injury. The pathophysiology of injury defines the patient's symptoms, examination findings, and treatment options and is critical to accurate diagnosis and treatment. The goals of treatment include management of the often associated pain and improvement of sensory and motor function. Understanding peripheral nerve anatomy is critical to adopting novel nerve transfer procedures, which may provide superior options for a variety of injury patterns.     

The lightning heart: a case report and brief review of the cardiovascular complications of lightning injury

Lightning strike is a rare natural phenomenon, which carries a risk of dramatic medical complications to multiple organ systems and a high risk of fatality. The known complications include but are not limited to: myocardial infarction, arrhythmia, cardiac contusion, stroke, cutaneous burns, respiratory disorders, neurological disorders, acute kidney injury and death. We report a case of a healthy young man who suffered a lightning injury and discuss the cardiovascular complications of lightning injury, ranging from ECG changes to death. The patient in our case, a 27-year old previously healthy male, developed a syndrome of rhabdomyolysis and symptomatic cardiogenic pulmonary edema. Electrocardiographic findings included transient T-wave inversions, late transition shift and long QT. His clinical condition improved with supportive measures.Early recognition of lightning injury syndromes and anticipation of complications may help us improve outcomes for these patients. Evaluation of patients having experienced a lightning injury should include a minimum of a detailed history and physical examination, 12-lead ECG and drawing of baseline troponins. Prolonged electrocardiographical monitoring (for monitoring of ventricular arrhythmias) and assessment for signs and symptoms of hemodynamic compromise may be warranted.     

Increased Expression of Apolipoprotein D Following Experimental Traumatic Brain Injury

Increasing evidence suggests that apolipoprotein D (apoD) could play a major role in mediating neuronal degeneration and regeneration in the CNS and the PNS. To investigate further the temporal pattern of apoD expression after experimental traumatic brain injury in the rat, male Sprague-Dawley rats were subjected to unilateral cortical impact injury. The animals were killed and examined for apoD mRNA and protein expression and for immunohistological analysis at intervals from 15 min to 14 days after injury. Increased apoD mRNA and protein levels were seen in the cortex and hippocampus ipsilateral to the injury site from 48 h to 14 days after the trauma. Immunohistological investigation demonstrated a differential pattern of apoD expression in the cortex and hippocampus, respectively: Increased apoD immunoreactivity in glial cells was detected from 2 to 3 days after the injury in cortex and hippocampus. In contrast, increased expression of apoD was seen in cortical and hippocampal neurons at later time points following impact injury. Concurrent histopathological examination using hematoxylin and eosin demonstrated dark, shrunken neurons in the cortex ipsilateral to the injury site. In contrast, no evidence of cell death was observed in the hippocampus ipsilateral to the injury site up to 14 days after the trauma. No evidence of increased apoD mRNA or protein expression or neuronal pathology by hematoxylin and eosin staining was detected in the contralateral cortex and hippocampus. Our results reveal induction of apoD expression in the cortex and hippocampus following traumatic brain injury in the rat. Our data also suggest that increased apoD expression may play an important role in cortical neuronal degeneration after brain injury in vivo. However, increased expression of apoD in the hippocampus may not necessarily be indicative of neuronal death.     

Head Injury and Early Signs of Tentorial Herniation: A Management Dilemma

In 100 patients intracranial exploration was done soon after severe head injury when signs of transtentorial herniation were present. A third of patients had extracerebral hematomas shown on initial burr hole examination. An additional 18 percent had parenchymal clots of clinical significance disclosed only by angiography after burr hole exploration or at autopsy. Half the patients in whom exploration was done did not have intracranial hematomas of sufficient size to warrant an operative approach. Detailed neurological examinations soon after injury and the availability of more rapid diagnostic tools may improve the accuracy of early diagnosis and allow more specific prognostication in patients with severe head injury.     

Questionable compensation claims; principles of special examination

In deciding a disputed claim of disability arising from occupation, physicians should ascertain whether a patient's medical history has any bearing on the disability; they should attempt psychologic evaluation of the patient as it may reflect on the conditions they observe in physical examination; they should investigate symptoms complained of by the patient rather than accept them as prima facie evidence of disability; and they must have knowledge of the extent to which an injury can cause disability. It is urged that standards of physical ability and disability, as well as of other physical factors which may affect compensation claims, be established by organized research.     

辛伐他汀对急性肺损伤及囊性纤维化跨膜传导调节体表达的影响

目的:探讨辛伐他汀对急性肺损伤大鼠囊性纤维化跨膜传导调节体(CFTR氯离子通道)的影响及其对减轻急性肺损伤的作用。方法:40只雄性SD大鼠随机分为空白组、模型组、辛伐他汀低剂量组(20 mg/kg)、辛伐他汀中剂量组(40 mg/kg)、辛伐他汀高剂量组(80 mg/kg);气道内滴注脂多糖(10 mg/kg)制备急性肺损伤模型。进行肺湿/干重比、肺泡灌洗液蛋白检测,HE染色观察肺组织的病理变化;实时荧光定量PCR检测肺组织匀浆CFTR mRNA表达。结果:结果显示,模型组的肺湿干重比,肺泡灌洗液蛋白较空白组高(P0.05),病理示肺泡膈增厚,大量炎性细胞浸润,肺泡腔内可见红细胞及血肿,提示模型复制成功。辛伐他汀低剂量组的肺湿/干重比、肺泡灌洗液蛋白与模型组相比无明显差异,病理可见肺损伤较重,与模型组相比无改善;CFTR mRNA表达与模型组相比稍高但无明显差异(P0.05)。辛伐他汀中高剂量组中肺湿/干重比、肺泡灌洗液蛋白与模型组相比有所降低,肺组织CFTRmRNA表达较模型组明显增加(P0.05),但中高剂量组之间无明显差异(P0.05);病理可见肺泡膈增厚,极少见炎性细胞浸润及透明膜,肺泡腔内未见明显出血和水肿,肺损伤程度较模型组减轻。结论:中高剂量的辛伐他汀(40 mg/kg)对急性肺损伤有一定保护作用,并上调CFTR的表达。     

QUESTIONABLE COMPENSATION CLAIMS—Principles of Special Examination

In deciding a disputed claim of disability arising from occupation, physicians should ascertain whether a patient''s medical history has any bearing on the disability; they should attempt psychologic evaluation of the patient as it may reflect on the conditions they observe in physical examination; they should investigate symptoms complained of by the patient rather than accept them as prima facie evidence of disability; and they must have knowledge of the extent to which an injury can cause disability.It is urged that standards of physical ability and disability, as well as of other physical factors which may affect compensation claims, be established by organized research.     

8-Br-cADPR, a TRPM2 ion channel antagonist,inhibits renal ischemia–reperfusion injury

The transient receptor potential melastatin-2 (TRPM2) channel belongs to the transient receptor potential channel superfamily and is a cation channel permeable to Na⁺ and Ca ²⁺. The TRPM2 ion channel is expressed in the kidney and can be activated by various molecules such as hydrogen peroxide, calcium, and cyclic adenosine diphosphate (ADP)-ribose (cADPR) that are produced during acute kidney injury. In this study, we investigated the role of 8-bromo-cyclic ADP-ribose (8-Br-cADPR; a cADPR antagonist) in renal ischemia–reperfusion injury using biochemical and histopathological parameters. CD38, cADPR, tumor necrosis factor-α, interleukin-1β, and myeloperoxidase (inflammatory markers), urea and creatinine, hydrogen peroxide (oxidant), and catalase (antioxidant enzyme) levels that increase with ischemia–reperfusion injury decreased in the groups treated with 8-Br-cADPR. In addition, renin levels were elevated in the groups treated with 8-Br-cADPR. Histopathological examination revealed that 8-Br-cADPR reduced renal damage and the expression of caspase-3 and TRPM2. Our results suggest that the inhibition of TRPM2 ion channel may be a new treatment modality for ischemic acute kidney injury.     

非肝炎病毒所致肝损害超声影像与病理关系的探讨

目的:对154例肝损害原因的超声与病理关系进行总结性分析,以提高对肝损伤的认知.方法:所有病例均行肝脏穿刺及病理检查,并结合临床相关特异性检查,明确肝损害的原因.结果:超声提示分别为肝损害、脂肪肝、肝纤维化、肝硬化,部分超声显示未见异常,病理结果提示在超声检查未见明显异常者中,部分确诊为代谢性疾病,超声提示肝损害组中,病理提示因药物、环境类生化因素所致肝损伤占有相当比例.结论:超声检查在肝损害的筛查中作用明显,而在肝损害原因中,药物性及环境类生化因素所致的肝损害占有相当比例.     

Fluorescence Microscopy of Fresh Tissue as a Rapid Technique for Assessing Early Injury to Mesophyll

A technique was developed for sectioning fresh red spruce foliage (Picea rubens Sarg.) for use in fluorescence microscopy. This allowed rapid examination of mesophyll in 3-5 mm needle sections. Healthy, ozone treated and cold stressed needles were examined to assess the utility of this technique for early detection of damage. Healthy mesophyll cells fluoresced bright red, while injured cells fluoresced yellow-green in ozone treated needles, and yellow-orange in frozen needles. Shifts in fluorescence wavelengths may be useful for early detection of injury to mesophyll before it is evident by standard light or electron microscopy.     

Protective effect of vitamin E on spinal cord injury by compression and concurrent lipid peroxidation

Studies were made on the influence of vitamin E on the effects of compression injury of the spinal cord associated with ischemia in rats. The motor disturbance induced by spinal cord injury was greatly reduced by vitamin E supplementation. After injury, the spinal cord evoked potentials showed greater recovery of both amplitude and latency in the vitamin E-supplemented group than in the control group. Spinal cord blood flow was promptly restored and remained normal after injury in the vitamin E-supplemented group, but was significantly decreased from 3 h after injury in the control group. Thiobarbituric acid (TBA)—reactive substances in the spinal cord was immediately increased by compression injury in both groups, and after injury it persisted at a high value for 24 h in the control group, but decreased within 1 h in the vitamin E-supplemented group. Pathological examination of the spinal cord showed less damage, such as bleeding and edema, in the vitamin E-supplemented group than in the control group. Vitamin E may have protective effects on the spinal cord by inhibiting damage induced by lipid peroxidation and/or by sustaining the blood flow by maintaining the normal metabolism of arachidonic acid.     

Inhibition of proliferation of fibroblasts by lazaroids (21-aminosteroids).

Lazaroids (21-aminosteroids) are a novel group of compounds that inhibit lipid peroxidation in biological systems and protect cells from oxidative damage during tissue injury. In vivo efficacy of lazaroids has been demonstrated in a variety of animal models of traumatic or ischemic injury of central nervous system (1-6). However, very little is known about the affects of lazaroids on cellular responses associated with tissue repair and remodeling eg cell proliferation and synthesis of extracellular matrix. In the present study, we show that lazaroids and certain related compounds inhibit cell proliferation in vitro. Light microscopic examination and determination of release of intracellular enzyme, lactate dehydrogenase suggested that cell growth inhibition by lazaroids was not due to cell death resulting from cytotoxic effects. Examination of several lazaroid related antioxidants and other known antioxidants eg vitamin E and Probucol showed that compounds with similar antioxidant potential did not exhibit identical antiproliferative activity, suggesting that cell growth inhibition by lazaroids may be unrelated to their antioxidant action. These results may have implication in the therapeutic actions of lazaroids.     

Baicalin attenuates focal cerebral ischemic reperfusion injury through inhibition of nuclear factor κB p65 activation

Baicalin is a flavonoid compound purified from plant Scutellaria baicalensis Georgi. We aimed to evaluate the neuroprotective effects of baicalin against cerebral ischemic reperfusion injury. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 24 h. Baicalin at doses of 50, 100 and 200 mg/kg was intravenously injected after ischemia onset. Twenty-four hours after reperfusion, the neurological deficit was scored and infarct volume was measured. Hematoxylin and eosin (HE) staining was performed to analyze the histopathological changes of cortex and hippocampus neurons. We examined the levels of NF-κB p65 in ischemic cortexes by Western blot analysis and RT-PCR assay. The results showed that the neurological deficit scores were significantly decreased from 2.0 ± 0.7 to 1.2 ± 0.4 and the volume of infarction was reduced by 25% after baicalin injection. Histopathological examination showed that the increase of neurons with pycnotic shape and condensed nuclear in cortex and hippocampus were not observed in baicalin treated animals. Further examination showed that NF-κB p65 in cortex was increased after ischemia reperfusion injury, indicating the molecular mechanism of ischemia reperfusion injury. The level of NF-κB p65 was decreased by 73% after baicalin treatment. These results suggest that baicalin might be useful as a potential neuroprotective agent in stroke therapy. The neuroprotective effects of baicalin may relate to inhibition of NF-κB p65.     

胰腺创伤的诊断和治疗进展

胰腺创伤的早期诊断是根据详细的询问病史、全面的体格检查,结合淀粉酶指标、B超、CT扫描、逆行胰胆管造影(ERCP)及磁共振下胰胆管成像(MRCP)等检查做出诊断,必要时应及时行剖腹探查,剖腹探查术是最可靠的早期诊断方法。依据损伤部位及严重程度,选择最佳的手术方式,可提高治愈率,减少并发症的发生,通畅引流是改善预后的关键措施,本文对胰腺创伤的诊治进展作一综述。